Sorghum Extract Enhances Caspase-dependent Apoptosis in Primary Prostate Cancer Cells and Immune Activity in Macrophages

Abstract

Sorghum bicolor L. is one of the important minor cereals in Asia, Africa, and the central United States, and it is considered a rich source of polyphenols, flavonoids, and dietary fiber. However, there is a lack of data on the anti-cancer activity of Sorghum in prostate cancer cells and immune activity in macrophages. This study aims to investigate the potential effects of an ethanol extract of S. bicolor L. (SE) on inducing apoptosis in RC-58T/h/SA#4 cells and immunomodulatory activity in RAW 264.7 cells. SE significantly inhibited the viability of RC-58T/h/SA#4 primary prostate cancer cells in a dose-dependent manner. The morphology of RC-58T/h/SA#4 cells treated with SE was shrunken and involved the formation of an apoptotic body and nuclear condensation. In addition, SE markedly activated caspase-8, -9, and -3; increased the protein levels of Bax, p53, cleaved PARP, and cytosolic cytochrome c; and decreased Bcl-2 protein expression. Furthermore, the inhibition of caspases in RC-58T/ h/SA#4 cells with z-VAD-fmk attenuated SE-induced cell growth inhibition. The production of nitric oxide (NO) was also elevated by SE treatment, as revealed by immune response parameters. These results suggest that SE inhibits growth and induces apoptosis in primary human prostate cancer cells in a caspase-dependent manner, and it modulates the immune functions in macrophages. Therefore, Sorghum bicolor L. may be used as a functional food to prevent prostate cancer and enhance immune activity.Key words : Apoptosis, immune activity, RC-58T/h/SA#4, Sorghum ethanol extract

Effects of Cirsium setidens extract on gene expression related to apoptosis induction and metastasis inhibition in human breast cancer

“…When phosphorylated p53 on the mitochondrial surface increases, the complex which is formed by Bcl-2, which promotes cell viability in the endogenous pathway, and Bax, a protein that liberates cytochrome c from mitochondria and induces apoptosis, is rearranged and apoptosis occurs through their antagonism (Jo et al, 2019). Therefore, the anticancer mechanism through apoptosis is the accumulation of phosphorylated p53 by the increase of AMPK in cancer cell, reducing Bcl-2 that inhibits apoptosis and increasing Bax that promotes apoptosis, resulting in loss of cell membrane potential and induces apoptosis through the destruction of the mitochondrial membrane and release of cytochrome c (Park et al, 2018;Cho et al, 2016).…”